Journal
ANNUAL REVIEW OF PLANT BIOLOGY, VOL 67
Volume 67, Issue -, Pages 261-285Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev-arplant-043014-114648
Keywords
TOR kinase; SnRK1 kinase; nutrient signaling; sugars; nitrogen
Categories
Funding
- Agence Nationale de la Recherche (ANR) [ANR-14-CE19-007, ANR-11-SV6-01002]
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo [FAPESP 2012/19561-0]
- Max Planck Society
- CAPES-COFECUB program
- Royal Society of New Zealand (Marsden Fund)
- MBIE
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All living organisms rely on nutrients to sustain cell metabolism and energy production, which in turn need to be adjusted based on available resources. The evolutionarily conserved target of rapamycin (TOR) protein kinase is a central regulatory hub that connects environmental information about the quantity and quality of nutrients to developmental and metabolic processes in order to maintain cellular homeostasis. TOR is activated by both nitrogen and carbon metabolites and promotes energy-consuming processes such as cell division, mRNA translation, and anabolism in times of abundance while repressing nutrient remobilization through autophagy. In animals and yeasts, TOR acts antagonistically to the starvation-induced AMP-activated kinase (AMPK)/sucrose nonfermenting 1 (Snf1) kinase, called Snf1-related kinase 1 (SnRK1) in plants. This review summarizes the immense knowledge on the relationship betweenTORsignaling and nutrients in nonphotosynthetic organisms and presents recent findings in plants that illuminate the crucial role of this pathway in conveying nutrient-derived signals and regulating many aspects of metabolism and growth.
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